Relationship of Adolescent Polycystic Ovary Syndrome to Parental Metabolic Syndrome

Leibel, Natasha; Baumann, Elizabeth; Kocherginsky, Masha; Rosenfield, Robert L.

doi:10.1210/jc.2005-1707

Cited by 109 publications

(71 citation statements)

References 76 publications

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“…To the best of our knowledge, nine studies have previously assessed the metabolic phenotypes of relatives of women with PCOS [13,[19][20][21][22][23][24][25]39]. The first of these studies concluded that glucose-stimulated hyperinsulinaemia was frequent in sisters (n=24) and brothers (n=5) of PCOS probands [19].…”

Section: Discussionmentioning

confidence: 99%

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Brothers of women with polycystic ovary syndrome are characterised by impaired glucose tolerance, reduced insulin sensitivity and related metabolic defects

Baillargeon

Carpentier

2007

Diabetologia

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Aims/hypothesis Since it has been shown that polycystic ovary syndrome (PCOS) is highly inherited and characterised by insulin resistance, we hypothesised that male siblings of PCOS women would also be insulin resistant. Thus, our aim was to assess insulin sensitivity and metabolic parameters in brothers of women with PCOS and male control individuals. Methods Seventeen brothers of PCOS women and 28 male control volunteers were assessed with 75 g OGTTs and euglycaemic-hyperinsulinaemic clamps. PCOS index women were identified using criteria developed at the 1990 National Institutes of Health conference. Results Brothers and control individuals were similar in terms of BMI, waist circumference, percentage body fat and BP. However, brothers had increased triacylglycerol (p=0.02), plasminogen activator inhibitor-1 (PAI-1; p=0.02), factor VIII (p=0.02), 2 h glucose (p<0.001), AUC glucose (p<0.001) and AUC insulin (p<0.001). Insulin sensitivity was reduced by 38% in brothers (p<0.001), and this was primarily due to a 65% decrease in insulin-stimulated non-oxidative carbohydrate metabolism (p<0.001). These differences remained significant after adjustment for age and BMI, except for triacylglycerol, PAI-1 and fasting glucose. The main findings also persisted after excluding individuals with impaired glucose tolerance or diabetic siblings. Significant interactions with BMI status were found for sex hormone-binding globulin, androstenedione, PAI-1 and AUC insulin , which were significantly altered only in obese brothers (vs control individuals). Conclusions/interpretation Brothers of PCOS women are characterised by decreased insulin sensitivity and glucose tolerance, as well as hypercoagulability, independently of obesity. Therefore, brothers of PCOS women may have inherited the insulin resistance and metabolic syndrome typical of PCOS.

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Section: Discussionmentioning

confidence: 99%

“…Few studies have assessed the metabolic phenotype of relatives of women with PCOS [13,[19][20][21][22][23][24][25], and only four of these assessed brothers [19][20][21][22]. These studies showed hyperinsulinaemia or altered indirect indices of insulin resistance in brothers, sisters, mothers or fathers of women with PCOS.…”

Section: Introductionmentioning

confidence: 99%

Brothers of women with polycystic ovary syndrome are characterised by impaired glucose tolerance, reduced insulin sensitivity and related metabolic defects

Baillargeon

Carpentier

2007

Diabetologia

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“…Moreover, there are data implying the linkage of adolescent PCOS with paternal metabolic syndrome (17). In order to identify the genetic factors resulting in the hereditary nature of PCOS, genes encoding enzymes involved in androgen synthesis (serine hyperphosphorylation of P450c17, 21hydroxy-lase (CYP21) mutation), or protein transducers of insulin signals (excessive phosphorylation of IR-beta, insulin receptor substrate (IRS) proteins, IRS-1 (Gly(972)Arg) and IRS-2 (Gly(1057) Asp) have been analysed (18,19).…”

Section: Genetic Factors Related To Pcosmentioning

confidence: 99%

What do we know about metabolic syndrome in adolescents with PCOS?

Cırık

Dilbaz

2014

J Turkish German Gynecol Assoc

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“…Paternal obesity not only impairs male fertility by impacting sperm count, motility and chromatin integrity [2][3][4][5][6][7] but also reduces subsequent embryo development, implantation rates, pregnancy success and live birth rates [8][9][10][11][12]. Interestingly metabolic syndrome, which includes obesity, in fathers is associated with polycystic ovary syndrome in daughters [13].…”

Section: Introductionmentioning

confidence: 99%

Female offspring sired by diet induced obese male mice display impaired blastocyst development with molecular alterations to their ovaries, oocytes and cumulus cells

Fullston

Shehadeh

Sandeman

et al. 2015

J Assist Reprod Genet

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Purpose To investigate the impacts that a paternal high fat diet (HFD) has on embryology, ovarian/cumulus cell gene expression and COC metabolism from female offspring, using a mouse model. Methods Founder male mice were either fed a control diet (CD) or a HFD for 12 weeks. The HFD induced obesity but not diabetes, and founder males were then mated to normal weight CD fed female mice. Female offspring were maintained on a CD, super-ovulated, mated and the resultant zygotes were cultured to the blastocyst stage for embryo morphology, blastocyst cell number and apoptosis assessment. Ovaries and cumulus cells from offspring were collected for gene expression analysis of selected genes that maintain chromatin remodeling and endoplasmic reticulum (ER), metabolic and inflammatory homeostasis. Cumulus/oocyte complexes were also investigated for glucose uptake and lipid accumulation. Results Female offspring sired by obese fathers produced embryos with delayed development and impaired quality, displayed increases in ovarian expression of Glut1, Glut3 and Glut4, and an increase in cumulus cell expression of Glut4. Interestingly their COCs did take up more glucose, but did accumulate more lipid. Conclusions A paternal HFD is associated with subfertility in female offspring despite the offspring being fed a CD and this subfertility is concomitant with ovarian/cumulus cell molecular alterations and increased lipid accumulation.

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Relationship of Adolescent Polycystic Ovary Syndrome to Parental Metabolic Syndrome

Abstract: Familial factors related to paternal MBS seem to be fundamental to the pathogenesis of PCOS.

Cited by 109 publications

References 76 publications

Brothers of women with polycystic ovary syndrome are characterised by impaired glucose tolerance, reduced insulin sensitivity and related metabolic defects

Brothers of women with polycystic ovary syndrome are characterised by impaired glucose tolerance, reduced insulin sensitivity and related metabolic defects

What do we know about metabolic syndrome in adolescents with PCOS?

Female offspring sired by diet induced obese male mice display impaired blastocyst development with molecular alterations to their ovaries, oocytes and cumulus cells

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